Canine respiratory diseases present a continuing heavy burden on dog populations. Due to ever changing patterns with little surveillance, and the emergence of new agents, we lack a clear understanding of the causative dynamics and interplay of this disease burden. The apparent recent increase in canine infectious respiratory disease complex (CIRDC) in the Unites States in 2023 and 2024 has resulted in many severe or even fatal events and substantial public alarm. Despite the widespread nature of the disease, we still do not understand the cause(s) of those outbreaks. However, one pathogen that has clearly contributed to CIRDC in recent years is the H3N2 canine influenza virus (CIV). An emergent virus in dogs, first identified in Asia 20 years ago, this virus has caused widespread outbreaks in dogs, including a large US outbreak from 2015-2017. We have been studying the evolutionary dynamics and epidemiology of H3N2 CIV and have found increased and sustained outbreaks of disease in US dog populations in recent years. Circulation of the virus appears most easily maintained within large-metropolitan shelter systems (e.g. Chicago, Dallas/Fort Worth, Philadelphia). But outbreaks and cases in boarding kennels and doggy day care centers likely also play a role, and outbreaks are often seen in smaller cities which generally die out after a month or two, but which may provide virus to interconnected regions. When infected dogs are present at large dog shows or agility meetings, the virus can also be spread widely as it can infect many dogs which then carry it to their home areas to cause additional outbreaks. The virus circulating in the USA currently has diverged genetically from the earliest strain that arose in China in 2004, and it also differs from the virus that was introduced into the USA in 2015 – which is still used in the current commercial vaccine (Merck).

Here we seek to better understand how the H3N2 CIV has circulated in the US over the past 9 years, with the goal to develop better control measures to allow viral eradication. Our sequencing studies have shown that the virus has been evolving steadily in dogs since it first emerged 20 years ago, and that mutations in different viral genes have become widespread and may be altering the viral fitness for growth and transmission in dogs. Our hypothesis is that some mutations result in the virus being better adapted to dogs, allowing both increased growth and more efficient spread. Some changes in the hemagglutinin (HA) surface protein may also result in antigenic variation that reduces the efficacy of the commercial CIV vaccine. We can directly test these hypotheses in laboratory virological studies of growth characteristics in cells in culture and in antigenic profiling. This project will therefore reveal foundational knowledge of a key player in CIRDC burden in dog populations, and lead to new strategies for CIV control in US dogs.